scholarly journals The physiological role of Cholecystokinin (CCK)-B/gastrin receptors in the gastric mucosal cell growth and the gastric acid secretion

2000 ◽  
Vol 82 ◽  
pp. 32
Author(s):  
Aki Nagata ◽  
Toshimitsu Matsui
1994 ◽  
Vol 267 (4) ◽  
pp. G702-G708 ◽  
Author(s):  
H. O. Jin ◽  
K. Y. Lee ◽  
T. M. Chang ◽  
W. Y. Chey ◽  
A. Dubois

Secretin has been known to inhibit gastric acid secretion in several species. However, the physiological role of secretin on the postprandial acid output and gastric emptying in an intact stomach remains controversial. In the present study, we reinvestigated the role of secretin in physiological dose range and endogenous secretin on gastric acid secretion and emptying in the stomach without influencing intragastric luminal pH in dogs. In seven conscious dogs with gastric cannulas, a 4% amino acid meal was administered intragastrically, and three different doses of secretin and an antisecretin serum were infused intravenously in each dog on separate days. Gastric emptying and net acid output were measured using a dye dilution technique, and plasma secretin and gastrin were determined by specific radioimmunoassays. After the meal, gastric emptying was exponential: acid output peaked at 25 min, and plasma concentrations of gastrin and secretin peaked at 15 and 60 min, respectively. Intravenous infusion of secretin at 1.25, 2.5, and 5.0 pmol.kg-1.h-1 dose dependently increased plasma levels of the peptide and suppressed postprandial plasma gastrin response and gastric acid output and emptying of the meal. Immunoneutralization of circulating secretin with a rabbit antisecretin serum abolished the postprandial rise of plasma secretin and significantly increased plasma gastrin, and augmented gastric emptying as well as acid output. It is concluded that, in dogs, secretin plays a physiological role in the regulation of gastric emptying and acid output after a liquid amino acid meal and that these effects may be mediated in part by suppression of the release of gastrin.


2001 ◽  
Vol 276 (49) ◽  
pp. 46436-46444 ◽  
Author(s):  
Andrea Todisco ◽  
Nonthalee Pausawasdi ◽  
Saravanan Ramamoorthy ◽  
John Del Valle ◽  
Rebecca W. Van Dyke ◽  
...  

2018 ◽  
Vol 154 (6) ◽  
pp. S-17
Author(s):  
Francesco Di Mario ◽  
Serena Scida ◽  
Marilisa Franceschi ◽  
Chiara Miraglia ◽  
Kryssia Rodriguez ◽  
...  

2003 ◽  
Vol 278 (38) ◽  
pp. 36470-36475 ◽  
Author(s):  
Jun Matsukawa ◽  
Kazuhisa Nakayama ◽  
Taku Nagao ◽  
Hidenori Ichijo ◽  
Tetsuro Urushidani

2001 ◽  
Vol 281 (4) ◽  
pp. G997-G1003 ◽  
Author(s):  
Arne K. Sandvik ◽  
Guanglin Cui ◽  
Ingunn Bakke ◽  
Bjørn Munkvold ◽  
Helge L. Waldum

Previous studies have shown that pituitary adenylate cyclase-activating peptide (PACAP) stimulates enterochromaffin-like (ECL) cell histamine release, but its role in the regulation of gastric acid secretion is disputed. This work examines the effect of PACAP-38 on aminopyrine uptake in enriched rat parietal cells and on histamine release and acid secretion in the isolated vascularly perfused rat stomach and the role of PACAP in vagally (2-deoxyglucose) stimulated acid secretion in the awake rat. PACAP has no direct effect on the isolated parietal cell as assessed by aminopyrine uptake. PACAP induces a concentration-dependent histamine release and acid secretion in the isolated stomach, and its effect on histamine release is additive to gastrin. The histamine H2antagonist ranitidine potently inhibits PACAP-stimulated acid secretion without affecting histamine release. Vagally stimulated acid secretion is partially inhibited by a PACAP antagonist. The results from the present study strongly suggest that PACAP plays an important role in the neurohumoral regulation of gastric acid secretion. Its effect seems to be mediated by the release of ECL cell histamine.


Physiology ◽  
1996 ◽  
Vol 11 (2) ◽  
pp. 57-62
Author(s):  
G Sachs ◽  
C Prinz

The interaction of gastrin, somatostatin, and other transmitters at the level of the histamine-containing enterochromaffin (ECL) cell is the major pathway determining rate of gastric acid secretion. Gastrin stimulates ECL cell elevation of [Ca2+]i, synthesis of histidine decarboxylase, histamine release, and cell growth by binding at a cholecystokinin-B receptor. Somatostatin inhibits gastrin-dependent elevation of [Ca2+]i and hence histamine release by binding to stomatostatin receptor 2 subtype.


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